Some
viruses encode proteins that promote cell proliferation while
others, such as the human immunodeficiency virus (HIV), encode
proteins that prevent cell division. It has been hypothesized
that the selective advantage determining which strategy evolves
depends on the ability of the virus to induce a cellular environment
which maximizes both virus production and cell lifespan. In HIV,
the protein that causes cell cycle arrest is Vpr.

Recently we developed a mathematical model based on discrete
difference equations (Holte S, Emerman M. to appear, Mathematical
Biosciences) to study the competition between two genotypes
of HIV---one that encodes this protein (Vpr+) and one that does
not (Vpr-). Recently, a team of students participating in the
2000 Industrial Mathematics Modeling Workshop for Graduate Students
at North Carolina State University extended this model to account
for the delay between cellular infection and the production
of new viral particles. In particular, we assessed the robustness
to perturbations of a number of parameters in the model. The
model will also be used to estimate a variety of parameters
from data produced in laboratory experiments.